These studies are designed to determine the mechanism of potassium transport in the intestine with emphasis on 1) potassium movement in the colon and 2) comparison with potassium transport in the distal tubule of the kidney. We have demonstrated that the administration of increased amounts of potassium in the diet results in an increase in Na-K-ATPase activity, the electrical potential difference and the potassium secretion in the colon. Similar changes were not observed in the jejunum. In further studies, potassium transport was studied in animals with renal insufficiency. Renal insufficiency did not alter Na-K-ATPase activity, electrical potential differences or potassium movement in animals fed normal intake of potassium. However, when the intake of potassium was increased to a level which did not alter potassium movement in normal animals, animals with renal insufficiency developed an increase in Na-K-ATPase activity, the electrical potential difference and potassium secretion. These studies strongly suggest that the movement of potassium is linked to Na-K-ATPase. Further studies of potassium transport have demonstrated that potassium adaptation i.e., the ability to excrete an increased potassium load following acute administration of potassium, occurs in the colon similar to the kidney during renal insufficiency and potassium loading. Further studies indicate that the colon unlike the renal tubule does not increase either sodium or water movement following the administration of vasopressin. These studies of potassium movement are continuing with emphasis on alterations of potassium movement during altered potassium intake and during administration of both glucocorticoids and mineralocorticoids. BIBLIOGRAPHIC REFERENCE: Fisher, K.A., Binder, H.J. and Hayslett, J.P.: Potassium Secretion By Colonic Mucosal Cells After Potassium Adaptation. Am. J. of Physiology 231:987-994, 1976.